Medical Journals

Carboxymethyl-chitosan Protects Rabbit Chondrocytes from Interleukin-1beta-induced Apoptosis.

Authors:
  • Chen Qing
  • Liu Shi-Qing
  • Du Yu-Ming
  • Peng Hao
  • Sun Li-Ping

From: Department of Orthopedics, Renmin Hospital of Wuhan University, Wuhan 430060, People’s Republic of China.

European journal of pharmacology

  • Publish Date: Jul 2006
  • ISSN: 0014-2999
  • Volume: 541
  • Issue: 1-2
  • Pages: 1-8
  • Medium: Print
  • Language: English
  • Citation (JAMA): Chen Qing, Liu Shi-Qing, Du Yu-Ming, et al. Carboxymethyl-chitosan Protects Rabbit Chondrocytes from Interleukin-1beta-induced Apoptosis.. Eur. J. Pharmacol. Jul 2006;541:1-8

Abstract

Chondrocyte apoptosis is important in pathogenesis of osteoarthritis. Chitosan is a non-toxic, biodegradable and biocompatible glycosaminoglycan. In this study, the effects of carboxymethyl-chitosan (CM-chitosan), a soluble derivative of chitosan, on chondrocyte apoptosis were investigated. Primary rabbit chondrocytes were cultured and induced to apoptosis by 10 ng/ml interleukin-1beta (IL-1beta). After treatment with various concentrations of CM-chitosan (50, 100, 200 microg/ml), the apoptotic rate, mitochondrial function, nitric oxide production, and the levels of inducible nitric oxide synthase (iNOS) mRNA and reactive oxygen species in IL-1beta-induced chondrocytes were examined. The results showed that CM-chitosan could inhibit chondrocyte apoptosis in a dose-dependent manner. Furthermore, it could partly restore the levels of mitochondrial membrane potential and ATP, decrease nitric oxide production by down-regulation of iNOS mRNA expression, and scavenge reactive oxygen species in chondrocytes induced by IL-1beta. The results suggested that the inhibitory effects of CM-chitosan on IL-1beta-induced chondrocyte apoptosis were possibly due to the protection of mitochondrial function, the decline in the levels of nitric oxide and reactive oxygen species.

Mesh Headings (Keywords): Adenosine Triphosphate, Animals, Apoptosis, Cell Nucleus, Cells, Cultured, Chitosan, Chondrocytes, Dose-Response Relationship, Drug, Flow Cytometry, Gene Expression Regulation, Enzymologic, Interleukin-1beta, Membrane Potentials, Mitochondrial Membranes, Nitric Oxide, Nitric Oxide Synthase Type II, RNA, Messenger, Rabbits, Reactive Oxygen Species, Reverse Transcriptase Polymerase Chain Reaction


Check for Full Text / PubMed Unique Identifier (PMID): 16740257


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